Neuro: Test 1 : Taube : Greatest Hits

Front 1

PT comes in with headache or other acute neuro findings in the ER

What is the first imaging study you want to use?

******

Back 1

NON CONTRAST CT

Front 2

What is one key reason why CT is better than MRI?

***

Back 2

it is good for quick evaluation of acute bleeding: Excellent for acute intracranial hemorrhage


(also, MRI might require pre-approval for access)

Front 3

where do epidural bleeds most commonly occur

Back 3

fronto-temporal area

Front 4

What is this? Where is it occuring

Back 4

Epidural bleed

frontal lobe

Front 5

what are the Hounsfield units for:
water
bone
air
blood
Fat

Back 5

0 = water density
+ 1000 = bone
-1000 = air
+ 60 – +80 = blood
- 5 to –12 = fat

Front 6

T1 vs T2 on MRI?

Back 6

T1 = the “anatomic” sequence
T2 = the “pathology” sequence


On T1 water is dark black
On T2 water is bright white

Front 7

T1 or T2?
What 4 things are black on this type of image?

Back 7

T1

Cortical bone
Bone
Moving blood
Fluid

Front 8

T1 or T2

Back 8

T2

Front 9

Which study, MRI or CT can detect ischemic injusry 24-36 hours earlier than the other?

Back 9

MRI

Front 10

This imaging study has no bone artifact (especially in the posterior fossa), and is better at assessment of tumors, white matter, and disease/early edema?

Back 10

MRI

Front 11

Which imaging study (CT or MRI) has unchanged multi-planar capability?

**

Back 11

MRI

Front 12

A 26 y/o patient presents to the ED after being struck by a softball bat. You want to rule our intracranial hemorrhage. You order:
A. CT
B. MRI

Back 12

CT (no contrast)

Cranial bone will be white

Front 13

Which modality is best for evaluating white matter disease?
A. CT
B. MRI

Back 13

MRI

Front 14

CT or MRI?

Back 14

MRI

Front 15

type of image? Path?

Back 15

Front 16

what normally causes an epidural hematoma?

Subdural?

Back 16

epi: skull fracture

sub: direct blow to the head w change in lvl of conciousness

Front 17

What happens in shear injuries?

Back 17

diffuse axonal injury

can be due to rotational injury (not necessarily blow to a head)

Front 18

path?

will it cross sutural lines?

what blood vessel causes it?

Back 18

epidural hematoma

DOESN'T CROSS SUTURAL LINES

assoc with skull fracture

due to arterial tear (middle meningeal artery)

Front 19

epidural hematoma vs subdural hematoma

which crosses suture lines?

Back 19

epidural hematoma :DOESN'T CROSS SUTURAL LINES

Sub: does

Front 20

for an epidural hematoma, at what amount of bleeding do you have to consider operative tx?

Back 20

less than 5mm: NON OPERATIVE

greater than 5mm: drain

Front 21

Back 21

epidural hematoma in kid

Front 22

describe some of the characteristics of subdural hematomas (shape, blood source, who it happens to)

Back 22

crecentic,
bridging veins,
old people who fall

Front 23

SDH more common with ____ while

EDH more common with _____

(cause of injury)

Back 23

SDH more common with falls
EDH more common with MVA

Front 24

Back 24

Subdural Hematoma

Front 25

Define the purpose of the Mental Status Exam

(o)

Back 25

Examination of neuropsychiatric functioning

Comprehensive description of a patient’s appearance, behavior, thinking, feeling, etc.

Meaningful only in the context of other baseline data (e.g., history, physical / neurologic exam)

Ex. Tearful patient may be reacting to stress or pain, be depressed, have neurological disease, or other cause

The MSE ≠ MMSE

Front 26

there are 3 densities seen on CT with a SDH..what are they and what are the time frames assoc with them

Back 26

Acute 0 to 3-4 days hyperdense

Subacute 3 to 20 days isodense

Chronic > 20 days hypodense

Front 27

Back 27

SDH

Front 28

Back 28

epidural hematoma

Front 29

this type of injury Occur with rapid acceleration/deceleration
Usually involves large WM tracts: corpus callosum, brainstem and deep white matter
Occurs at gray-white matter interface due to slight differences in mass
Minor differences in tissue inertia

Back 29

Shear Injuries

Front 30

Back 30

Intraparenchymal hemorrhage from shear injuries

Front 31

Back 31

MRI showing
intra parenchymal
hemorrrhage

Front 32

Left Middle Cerebral Artery Infarction with midline shift:

what is the most useful landmark for measuring midline shift?

Back 32

Most useful landmark for measuring midline shift: Septum Pellucidum

note:This type of edema is called cytotoxic edema


cytotoxic edema visible on CT and MRI

Front 33

what is key to remember about cytotoxic edema?

Back 33

Affects both gray and white matter

Front 34

History: stroke symptoms

Back 34

cytotoxic edema

Front 35

Explain how the Mental Status Exam is performed

(o)

Back 35

By observation
i.e., many areas assessed while obtaining the history
e.g., speech, behavior, affect

By asking relevant questions to elicit symptoms that usually cannot be observed
e.g., hallucinations, paranoid ideation, mood

By performing cognitive screening tests
e.g., MMSE, other bedside tests

Front 36

vasogenic edema is found where?

cytogenic?

causes?
***

Back 36

vasogenic edema: CONFINED TO WHITE MATTER (tumor or infection)

where cytogenic could be in white or gray (infarct or stroke)

Front 37

SUMMARY SLIDE

CT is 1st in the emergent setting to rule out hemorrhage.
MRI is more sensitive for edema, tumors, infections and white matter disease.
Be able to distinguish SDH from EDH.

Be able to distinguish cytotoxic (stroke) from vasogenic (tumor or infection)

Back 37

CT is 1st in the emergent setting to rule out hemorrhage.--FAST

MRI is more sensitive for edema, tumors, infections and white matter disease.--CONTRAST MAKES IT EVEN MORE SENSITIVE

Be able to distinguish SDH from EDH.--SDH more cresentic, covers further distance, not confined by sutures

Be able to distinguish cytotoxic (stroke-effects both grey and white matter) from vasogenic (tumor or infection--just in white matter)

Front 38

Identify the major components of the Mental Status Exam

(o)

Back 38

General appearance, attitude (toward the examiner), and behavior

Motor activity (overactivity, underactivity, abnormal movements, catatonia)

Speech

Mood and affect

Thought process (form) and content

Perception

Cognitive function

Insight and judgment

Front 39

What is the difference btw catatonia, catalepsy, and cataplexy?

***

Back 39

Catatonia: motor symptom: Dx by any two of the following: a. motor immobility, b. motor excitement, c. negativism or mutism, d. posturing, stereotypies or mannerism, e. echolalia (parroting) or echopraxia (miming)

Catalepsy: feature of catatonia, waxy flexibility (muscular rigidity and fixity of posture regardless of external stimuli, as well as decreased sensitivity to pain.)

Cataplexy: sudden loss of muscle tone leading to collapse, related to narcolepsy

Front 40

describe the following mood/affects

Constricted/Restricted (flat)
Labile
Expansive

Back 40

Front 41

define the following disturbances in thought process:

Circumstantiality
Tangentiality
Looseness of associations
Verbigeration
“Word Salad”
Neologisms
Clang associations

Back 41

Circumstantiality (excessive detail but gets to point)
Tangentiality (never gets to point of message)
Looseness of associations (ideas loosely connected)
Verbigeration (meaningless repetition of words/phrases)
“Word Salad” (incoherent collection of words/phrases)
Neologisms (creation of new words)
Clang associations (rhyming/punning; no logical connection)

Front 42

describe circumstantial thought

*board fodder

Back 42

Front 43

Describe Tangential thought

*

Back 43

Front 44

Describe flight of ideas

*****

Back 44

Front 45

what is the difference between hypnagogic and hypnopompic hallucinations? are these pathological or non pathological?

***

Back 45

Nonpathological: hypnagogic (when you go to sleep), hypnopompic (when you wake up)

Pathological: Auditory, visual, tactile, olfactory, gustatory, somatic

Front 46

what are
Perceptual disturbances? (4)

****

Back 46

include:
hallucinations,
derealization (where I am at doesn't feel real, i am floating in the space I am in),
depresonalization (feel like you are floating outside of yourself),
déjà vu

Front 47

One-half of all lifetime cases of mental illness begin by age...

Back 47

14

three-quarters by age 24.

Front 48

on the MMSE what score points to cognitive problems?

Back 48

less than 20

Front 49

Recognize the difference between the Folstein MMSE and the mental status examination

(o)

note: answer extrapolated from Wiki

Back 49

The mini–mental state examination (MMSE) or Folstein test is a brief 30-point questionnaire test that is used to screen for cognitive impairment. It is commonly used in medicine to screen for dementia. It is also used to estimate the severity of cognitive impairment at a given point in time and to follow the course of cognitive changes in an individual over time, thus making it an effective way to document an individual's response to treatment.

Mental status is way more in depth

Front 50

What are illusions (with respect to perceptual disturbances?)

**

Back 50

misinterpretation of real stimuli

Front 51

Define psychiatric illness

(o)

Back 51

Any of various conditions characterized by impairment of an individual's normal cognitive, emotional, or behavioral functioning, and caused by social, psychological, biochemical, genetic, or other factors, such as infection or head trauma.

Also called emotional illness, mental illness, mental disorder.

Front 52

what is the difference btw primary and secondary psychiatric disorders?

Back 52

Primary psychiatric disorders
No underlying medical disorder to account for the diagnosis
Not caused by medication
Not caused by substance abuse or withdrawal

Secondary psychiatric disorders
Due to a medical condition
Due to a medication(s)
Due to substance abuse or withdrawal

Front 53

Identify the domains of psychiatric illness (6)

(o)

Back 53

Some People Can Eat Bad Eggs

Front 54

Identify the classification systems used to diagnose psychiatric illness

(o)

Back 54

Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR)
Published by the American Psychiatric Association (2000)
Most recent update of criteria: DSM-IV (1994)
Current DSM bases diagnostic codes on ICD-9-CM

International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM)
Published by the US government in 1979
Official coding system in the US for all diseases (Ch.5 Mental Dis)
Revises codes annually but has not kept up with diagnostic changes in the DSM

Front 55

What is an important thing to remember about the DSM IV and diagnosis it gives

****

Back 55

Contains a listing of psychiatric disorders, diagnostic codes, and criteria for each disorder

Also contains text with information about the disorder (e.g., associated features, prevalence, course, familial patterns, age-,culture- and gender-specific features, differential diagnosis)

***Does NOT contain information about presumed etiology or treatment****

Front 56

Describe the DSM-IV-TR multiaxial diagnostic system

(o)

Back 56

Axis I: Clinical Disorders (psychiatric)

Axis II: Personality disorders and traits, mental retardation, prominent defense mechanisms

Axis III: General Medical Conditions

Axis IV: Psychosocial and environmental problems (stressors)

Axis V: Global Assessment of Functioning (1-100 scale)


EXAMPLE
Axis I 296.22 Major Depressive Disorder, single episode, moderate
305.00 Alcohol Abuse

Axis II 301.6 Dependent Personality Disorder

Axis III Hepatitis B

Axis IV Threat of job loss

Axis V GAF = 45 (current)

Front 57

explain why most mechanisms of action given the neuropharmacologic drugs are approximations.

(o)

Back 57

Entire mechanism is generally unknown. Approximations of

CNS mechanism made from information regarding effects of drugs in isolated systems.
CNS as a “Black Box”
Extrapolation from biochemical events to behavior is difficult.

Front 58

Identify the components of a psychiatric evaluation

(o)

Back 58

History (Identifying Data/Reason for admission or evaluation, Past Psychiatric History, Substance History, Mental Status Exam)




Exam (neuro/mental)

Radiological and lab

Front 59

SUMMARY SLIDE FOR LECTURE 2 OF PSYCH

Back 59

Psychiatric symptoms can be seen in many conditions

The etiology of most primary psychiatric disorders is not known

Diagnosis is based primarily on history and mental status exam

Physical exam, neurologic exam, lab, and other studies are performed to rule out possible non-psychiatric causes of psychiatric symptoms

The DSM-IV-TR increases reliability of diagnosis

Front 60

define what is meant by specific mechanism of action.

(o)

Back 60

A specific drug action affects a recognized protein target, i.e., a receptor, an ion channel, an enzyme, or a transporter.

Front 61

describe the various events in synaptic transmission which might be altered by drugs

(o)

Back 61

Front 62

The student will be able to explain and account for differences in brain-injury patterns caused by high- and low-velocity missiles.

(o)

Back 62

k.e.= ½ m v2

so the faster the traveling bullet (military weapon) will be more likely to kill you than a slow moving bullet (civilian weapon)

Front 63

please define a concussion

(o)

Back 63

Diffuse, physiological and microscopic insult, with or without diffuse axonal injury

Usually defined as involving a period of confusion or unconsciousness, even if just brief

Numerous common associated symptoms, e.g. headache, dizziness, irritability, emotionality, poor concentration

Front 64

what is the difference between a neurotransmitter and a neuromodulator?

(o)

Back 64

Neurotransmitter – a substance which is released locally and causes a change in post-synaptic potential.

Neuromodulator – a substance which acts to modify the response of the synapse to a neurotransmitter. (make a stimulus stronger or weaker)

Front 65

highschool football player gets hit on the head in the second half of the game and dies. Why did this happen? this is an example of?

*

Back 65

You look back and see that the kid got hit on the head in the 1st half but it was dismissed or not realized

the SECOND IMPACT SYNDROME says that the brain is waaayyyy more vulnerable to a 2nd injury

this is more common in younger ppl

Front 66

recognize the substances which have been proposed to act as CNS neurotransmitters

(o)

Back 66

Acetylcholine
Amino acids
Biogenic amines
Peptides
Purines (ATP, adenosine)
Nitric acid
Endocannabinoids

Front 67

differentiate between ionotropic and metabotrophic receptors.

(o)

Back 67

Ionotropic receptors (also known as ligand-gated ion channels) are associated with ion channels, and change ionic conductance.
Mediate fast, short effects.

Metabotropic receptors are coupled with enzymes via G-proteins and other intermediates.
Mediate slow, long effects.

Front 68

describe the blood brain barrier and its implications in drug therapy (what are the characteristics that regulate diffusion of substance through capillaries)

(o)

Back 68

A term used to describe diffusional barriers retarding the passage of substances from the central circulation to nerve cells.

Characteristics which regulate diffusion of substances through capillaries are:

Molecular weight
Lipid solubility
Ionization at physiological pH (ionized drugs are not lipid soluble)

Front 69

Little Johnny gets hit in the head during a game and gets knocked out. Mom and Dad bring him to you and ask if he can play the next game in 2 days. What do you tell them

Back 69

have to be at least a week of no symptoms before they can resume play

Front 70

pleas define a brain contusion..where do they tend to occur?

(o)

Back 70

Focal hemorrhages within brain tissue
Big enough to see with naked eye in a pathology specimen or as an area of intensity (whiteness) on a CT scan
Tend to occur around edges of brain, particularly at base of cerebrum and in anterior temporal lobes

Front 71

describe a subdural hematoma including the location, and appearance on CT initially and chronically

(o)

Back 71

Traumatic hemorrhage from veins inside dura but outside brain

This behaves like an actual space, so, acutely, blood runs from anterior to posterior pole

The hematomas appear initially white (X-ray dense) on CT

Over time, the hematomas get diluted and resorbed, and become less X-ray dense

Front 72

describe an epidural hematoma including the location, and appearance on CT initially and chronically...what is the cause?

(o)

Back 72

Traumatic hemorrhage from meningeal arteries inside skull but outside dura

This is a potential space through which the fresh blood dissects from edge to edge, creating a lens-shaped hematoma that does not extend from pole to pole (the subdural does)

The hematomas appear white (X-ray dense) on CTs acutely, but become less dense as they dilute and resorb

Front 73

please describe the Glasgow Coma scale, including the 3 aspects, and scoring ranges

Back 73

Front 74

define epilepsy...

incidence?

Back 74

2 or more unprovoked seizures

incidence is highest in kids and old folk

Front 75

in-between epileptic seizures, what is a common finding on EEG?

Back 75

Spikes

Front 76

What happens in an absence seizure? clinically and EEG

(o)

Back 76

Clinic: pt suddenly stops responding/no eye contact for about 7 seconds and then just resumes back to normal (full recovery)

EEG: sudden spiking in all leads, quick onset, quick ending

Front 77

What happens in a tonic-clonic seizure? clinically and EEG

(o)

Back 77

Clinic: abrupt onset with no warning, pt starts arching back (tonic) and then clonic (shaking all over), NO IMMEDIATE RECOVERY, pt might have pissed themselves, bit their tongue, want to go to bed--this is what you classically think of as a seizure

EEG: sudden rapid hashy spiking (tonic) in all leads, followed by spike then pause, spike then pause (in all leads) leading to the jerkiness (clonic). When the seizure ends, the EEG is not completely normal (shows the disorientation when it ends)

Front 78

What happens in a Partial Simple Seizure? clinically and EEG

(o)

Back 78

specific to what brain area is affected

for example, a pt could have a left motor seizure causing a right arm tremor. Pt is wide awake, aware of the symptoms, but can't stop them

EEG: Will only see irregular activity in certain leads (that correspond to one side of the brain, thus focal)

Front 79

What happens in a Partial Complex Seizure? clinically and EEG

(o)

Back 79

occurs in the Temporal lobe

usually clouding of consciousness

EEG: Will only see irregular activity in certain leads (that correspond to one side of the brain, thus focal)
Can occur in 4 places:
anterior-deja vu/psychic symptoms
Sylvian- Epigastric sensation, movement of mouth and face
Mid-temporal - auditory hallucinations, depersonalization
posterior temporal-Complex visual hallucinations

Front 80

a pt says every now and then I keep seeing a pack of wild dogs that nobody else can see...what is this?

Back 80

Partial-Complex Seizure

Front 81

what is common and similar in Absence and Partial Complex Seizures
Consider:
brain involvement
Age of pt
Duration
Sx recalled by pt
Movements or behaviors
After-effects
EEG pattern
Underlying Cause
Effective Tx

TEST!!!!!!!!!!!!!!!!!!!!!!!!!

Back 81

ONLY THING SHARED: STARING AND DECREASED RESPONSIVENESS

Front 82

The student will be able to correlate the age of onset of first seizure with likely underlying causes.
Consider:
Idiopathic
Febrile
Birth Injury
Metabolic
Infection
Trauma
Tumor
Stroke

(o)

Back 82

Front 83

The student will be able to describe the means and rationale for investigation of a new seizure disorder by history, examination and ancillary testing.-JUST READ

(o)

Back 83

CBC—is there an elevated white count to imply infection?
Chemistries—especially glucose, sodium, calcium, renal function tests and liver function tests.
Brain imaging to look for macroscopic focal disease, such as tumor, stroke, arteriovenous malformation or developmental anomaly.
An MRI scan including coronal sections through the medial temporal lobes is ideal, but there are circumstances in which a CT is substituted, e.g. when the patient is restless, claustrophobic or has a pacemaker.
An EEG, preferably sleep-deprived to increase sensitivity. Does the EEG show abnormalities, especially spikes, highly associated with seizures? If so, are they focal or generalized?

Front 84

pt presents with multiple cognitive deficits including memory impairment, aphasia, apraxia (arm won't do what you tell it to), agnosia (trouble remembering what objects are), or trouble in executive functioning (have trouble cooking). What do they have?

(o)

Back 84

Alzheimer's Dz

note: the shrinking effect on the brain is bigger due to age than Alzheimers (like an 80 year old with AD would have a larger brain than a normal 90 year old)

Front 85

on a PET scan, what will be a difference seen in a pt with Alzheimer's dz?

Back 85

less activity posteriorly

Front 86

amyloid plaques are commonly seen on silver stain in what? what is another pathological finding of this problem?

Back 86

Alzheimer's Dz

Neurofibrillary Tangles (used to be neurotubules, will be in the cells)

Front 87

What are 2 pharmacological tx for AD?

Back 87

Acetylcholinesterase Inhibitors [Examples: Donepezil (Aricept) Galantamine (Reminyl, Razadyne)
Rivastigmine (Exelon)] --used in mild to moderate disease

NMDA (Glutamate) Receptor Blocker (Memantine (Namenda))-- Moderate level of disease

Front 88

Progressive dementia clinically similar to Alzheimer’s disease

Early, prominent involvement of frontal and temporal lobes (“frontotemporal dementia”)

(o)

Back 88

Pick's Disease

will find Pick Bodies intracellularly

note: PET scan will show less activity in the frontal and temporal lobes (who'da thought)

Front 89

Hypokinesia/akinesia
Bradykinesia
Rigidity (not to be confused with spasticity or paratonia)
Stooped posture
Small-stepped gait
“Rest” tremor, typically unilateral or asymmetric

area all seen in what?

Back 89

Parkinsonism

Front 90

associated with degeneration of substantia nigra cells containing intracellular Lewy bodies

(o)

Back 90

Parkinson's Disease

Front 91

Usual fluctuations in cognitive function, involving alertness and attention
Visual hallucinations are common
Will also have movement problems
Pathologically, intracellular Lewy bodies appear diffusely in the cerebral cortex

(o)

Back 91

Dementia with Lewy Bodies

Clinically resembles a blend between Alzheimer’s and Parkinson’s diseases

note: in Parkinson's, the Lewy Bodies are mostly in the Substantia Nigra

Front 92

(o)

Back 92

Front 93

flip for a comparison of dementia with Lewy Bodies, Alzheimer's Disease, Parkinson's

Back 93

Front 94

pt presents to your office due to changes in mood. Upon walking you notice that they seem to flick their hand, or kind of dance around. What is this? Genetics?

(o)

Back 94

Huntington’s Disease

Autosomal dominant with high penetrance
Abnormal gene on chromosome 4

note: the dancing/flicking movement is known as CHOREA

Front 95

What change in the brain would you see in a pt with Huntington's disease?

Back 95

Absence of the Caudate Nucleus

Front 96

A rapidly progressive, fatal dementia involving prominent motor symptoms, such as rigidity, clumsiness, and myoclonic jerks
A transmissible “spongiform” encephalopathy involving abnormal proteins called prions
Diagnosed with certainty only by brain biopsy

(o)

Back 96

Creutzfeldt-Jakob Disease

Front 97

What are the 3 categories of Creutzfeldt-Jakob Disease? Which are we most concerned about?

Back 97

Sporadic CJD appearing without known risk factors accounts for 85% of cases.

Hereditary CJD involves positive family history or positive testing for a genetic mutation. 5-10% of U.S cases.

Acquired CJD involves transmission by exposure to brain or nervous system tissue. 1% of cases. (****transmission from open wounds, retina transplant, etc)

Front 98

Increased levels of CSF protein 14-3-3 would give you the diagnosis of?

Back 98

Creutzfeldt-Jakob Disease

Front 99

inflammatory demyelinating plaques in the central nervous system is the hallmark of what?

(o)

Back 99

Multiple Sclerosis (MS)

has to do with OLIGODENDROCYTES (not Schwann--peripheral)

Front 100

T1 “Black Holes” and brain atrophy can be seen in what?

Back 100

Multiple Sclerosis

note: Gilenya ™ - Fingolimod is the first oral pill tx for MS

Front 101

2. The student will be able to correlate brain tumors and their usual anatomic compartments.

3. The student will be able to provide examples of brain tumors that are more or less common in younger and older patients.

(o)

Back 101

Front 102

midline tumors and tumors of cerebellar lobes are more common in adults or kids?

Back 102

kids

Front 103

this is the Fastest-growing and most lethal brain tumor in astrocytoma series
Infiltrates and spreads widely within brain, so surgery cannot entirely remove
Surgery still warranted for biopsy, with or without de-bulking and insertion of Gliadel wafer
Radiation therapy usually applied

*

Back 103

Glioblastoma Multiforme

Front 104

this brain tumor is chiefly in adults 30-50, has Intermediate growth rates depending on grade, can sit dormant for years with no effect. Radiation therapy can be applied, but is usually reserved for when the tumor is perceived as growing because there is a lifetime limit to how much can be given.

Back 104

Cerebral Astrocytomas

Front 105

Usually the slowest growing brain tumors, but can eventually crowd the brain.
Often discovered as an incidental finding on a scan done for another reason
Are usually calcified and are therefore very recognizable on CT scans.

Back 105

Meningiomas

Front 106

please give an example that fits each of the following:
A fast-growing intracranial tumor displaces brain.

A slow-growing intracranial tumor replaces brain

Back 106

A fast-growing intracranial tumor displaces brain. (Examples: glioblastoma multiforme, metastases.)

A slow-growing intracranial tumor replaces brain. (Example: typical meningioma.)

Front 107

Most frequent incidence between ages of 30 and 50
Also calcify and usually show this on CT scans.
Intermediate growth rate, and is usually "managed" (surgery, RT) rather than cured
Glial cell in origin

Back 107

Oligodendrogliomas

Front 108

Can be hormonally active or disruptive
Can compress optic chiasm from below and produce visual field losses
Often removed surgically through the nose and sphenoid sinus

Back 108

Pituitary Adenomas

Front 109

what are some of the important areas that can be damaged by occluding the middle cerebral arteries?

Back 109

Broca/Wiernicke's

Motor/Sensory cortex

Frontal eyelid

Optic radiation... others

Front 110

Comprise about 1/3 of childhood posterior fossa tumors
Predilection for cerebellar vermis
Though malignant, they are highly radio-sensitive

Back 110

Medulloblastomas

Front 111

posterior fossa tumor of childhood
Often encapsulated
Complete surgical extirpation often possible

Back 111

Cerebellar Astrocytoma

Front 112

2 of the most common primary cancers in existence are what? so what can this lead to?

(o)

Back 112

breast and Lung

can lead to brain (intermediate tenancy to go to the brain)

Front 113

The student will be able to describe more and less common sources of metastatic brain tumors.

aka what are the most and least likely to go to the brain***

(o)

Back 113

Prostate: DOES NOT go to brain

Melanoma: GOES TO BRAIN (very high propensity)

Front 114

The student will be able to describe treatments for tumors of the nervous system as well as their optimum applications and limitations. What are the options (4)

(o)

Back 114

High-dose corticosteroids
Surgery
Radiation therapy
Chemotherapy

Front 115

How do high dose corticosteroids help treat brain tumors?

(o)

Back 115

Buys time by shrinking the edema around the tumor deposit, rather than affecting the tumor itself.
Effective against extracellular edema, but not intracellular edema, such as that seen in ischemia.
A typical starting dose is dexamethasone 10 mg, followed by 4 mg q.i.d

Front 116

how does radiation therapy help treat CNS tumors?

(o)

Back 116

RT is usually palliative--to shrink but not eliminate tumor deposits
For brain metastases, RT is sufficiently effective that the patient usually dies of non-CNS complications before CNS complications.
The treatment itself can damage the CNS.

Front 117

When do you often see chemotherapy for CNS tumor treatment?

(o)

Back 117

Usually reserved for glioblastoma multiforme (Fastest-growing and most lethal brain tumor in astrocytoma series
Infiltrates and spreads widely within brain, so surgery cannot entirely remove)


IV administration is complicated by intact blood-brain barrier blocking entry into CNS.
BCNU (carmustine) given IV probably crosses BBB to some extent.
Gliadel® wafers (also carmustine) can be implanted within the tumor bed.

Front 118

anterior cerebral artery blockage can lead to problems where

Back 118

leg and foot of motor and sensory

Front 119

Posterior cerebral artery occlusion will give you what major problem?

Back 119

visual deficits

Front 120

non-traumatic Subarachnoid Hemorrhage is normally due to what?

Back 120

aneurysm

Front 121

where do aneurysms typically occur? (berry)

Back 121

close to the circle of willis

most in Anterior communicating (like in marfans)

Front 122

besides trauma, what are the 2 major causes of intraparenchymal hemorrhage?

(o)

Back 122

Hypertension-associated

Arterio-venous malformation (AVM)

note: this is literally bleeding into brain tissue

Front 123

where do Charcot-Bouchard microaneursyms occur? how are these different from Berry aneurysms

*

Back 123

on penetrating arteries (deep in the brain, leading to areas like the basal ganglia)--assoc with intraparenchymal hemorrhage

different from saccular (Berry) aneurysms occurring near the circle of Willis. assoc with subarachnoid hemorrhage

Front 124

large wedge shaped damage vs small pockets of damage...

please list what type of vessels were damaged

(o)

Back 124

Wedges: large vessels

small pockets/lacunae: small (will be in penetrating arteries

Front 125

what is the difference between an embolism and thrombosis

(o)

Back 125

embolism: some garbage from upstream got dislodged, then it gets stuck in the brain

thrombosis: clot...can lead to breaking off and causing an embolism

so: embolism arises from somewhere else, thrombus occurs from the site

Front 126

what is most commonly going to cause an embolism?

Back 126

Atrial fibrillation

(irregularly irregular)

Front 127

what is the concept of ischemic penumbra?

*

Back 127

There is a central core of forever-lost brain cells that no treatment can revive surrounded by a larger zone of sick brain cells that may or may not recover – depending on acute management.

Front 128

in stroke, what effect can blood sugar have on acute stoke management?

Back 128

Too high can be damaging!!

Front 129

what are some of the modifiable atherosclerotic risk factors? 4 (+1 non-modifiable)

(o)

Back 129

Blood pressure
Blood sugar
Lipids (statin drug)
Smoking


note: Family History

Front 130

shortly after stroke it is important to monitor BP. If it is really high what should you do? Should you let a pt walk right away?

Back 130

we lost autoregulation, so be careful not to drop BP too aggressively-->can extend the stoke

so if their BP is high, don't worry about it for the immediate time being

also, don't let them walk, they may have an unsafe drop in BP

Front 131

if you are going to give a drug for acute treatment of thrombotic stroke, which of the following would you use?

t-PA
heparin
aspirin

Back 131

ASPIRIN has small benefit acutely

note: heparin would be good to prevent DVT from bed rest

Front 132

what commonly causes stroke for old and young folks?

(o)

Back 132

old folks: atherosclerosis or emboli from heart

young folks: congenital heart/great vessel defects; hypercoaguable states, migraine with aura + smoking + contraceptives

Front 133

Giant Cell Arteritis
Tumor
Subarachnoid Hemorrhage
Subdural Hematoma
Epidural Hematoma
Medication Overuse Headaches

are examples of what type of headache?

(o)

Back 133

Secondary Headaches

Front 134

a pt shows up with really bad headaches and insists they have a tumor that is causing it. You respond..

Back 134

they are extremely rare, and not likely the cause of your headache

Front 135

What is a medication overuse headache?

(o)

Back 135

person needed to take medicine for a headache

they took it too often for a long enough time

you transform it into a 2ndary headache that is more difficult to treat

headaches will occur everyday, present throughout the whole day, and is mild to moderate. It worsens when the medication is discontinued

Front 136

an elderly female presents to your office with a unilateral headache, jaw claudication and impaired vision. What does this pt have? is this a primary or secondary headache? FIRST AID REVIEW: What is the tx??

(o)

Back 136

Giant cell arteritis

secondary

High dose steroids

Front 137

Migraine without Aura
Migraine with Aura
Tension-Type Headaches
Cluster Headaches

are what kind of headaches?

(o)

Back 137

Primary

Front 138

pt presents with a unilateral headache that feels like it is "pulsing". They say it is aggravated with activity and they have some nausea. They say they only have light sensitivity some of the times when this occurs...what is it?

Back 138

Migraine without aura

Front 139

what are some of the common triggers for migraines?

Back 139

Hormonal – menstruation, ovulation, OCP, HRT
Dietary – alcohol, nitrite-laden meat, MSG, aspartame, chocolate, aged cheese, missing a meal
Psychological – stress, post-stress let-down, anxiety, worry, depression
Physical/Environmental – glare, flashing lights, visual stimulation, fluorescent lighting, odors, weather changes, high altitudes
Sleep-related – lack of sleep, excessive sleep
Miscellaneous – head trauma, physical exertion, fatigue
Drugs – NTG, histamine, reserpine, hydralazine, ranitidine, estrogen

Front 140

what is the most common aura in migraines with aura? some examples?

Back 140

VISUAL

scotomas (blind spots), photopsia (unformed flashes of light), fortification spectra (scintillating zig-zag lines), distortions in shape and size. In “retinal migraine,” these occur unilaterally instead of bilaterally.

Front 141

what are the 5 types of migraine auras?

Back 141

Visual: scotomas (blind spots), photopsia (unformed flashes of light), fortification spectra (scintillating zig-zag lines), distortions in shape and size. In “retinal migraine,” these occur unilaterally instead of bilaterally.

Somatosensory: unilateral paresthesias (spontaneous sensations) or hypesthesia (decreased perception of applied stimuli).

Motor: hemiparesis.

Language: aphasia (impairment of language comprehension or expression).

Brainstem: loss or change in level of consciousness, diplopia, tinnitus or hearing loss, vertigo, dysarthria, ataxia, bilateral sensory or motor symptoms.

Front 142

pt comes in with a mild/moderate pressing headache that is bilateral. It does not get worse with activity and there is no nausea associated with it...what is this?

(o)

Back 142

Tension type headache

THE ANTI MIGRAINE (pretty much the opposite: no light sensitivity, no nausea, doesn't get worse with activity)

Front 143

what does the "cluster" refer to in cluster headache?

Back 143

The "cluster" means clustering in time (not location)

Front 144

pt presents with recurrent headaches occurring around the the eye lasting for about 15 minutes to 2 hours. He says the pain is intense but then goes away. What is this?

(o)

Back 144

Cluster headache

Front 145

Clumsiness in greater proportion than loss of power
Babinski sign present (immediate)
Spasticity (delayed)
Increased tendon reflexes (delayed)
Little if any atrophy

what type of lesion?

(o)

Back 145

Upper motor neuron lesion

Front 146

what is Spasticity...what is it associated with (upper or lower mn)

(o)

Back 146

A unidirectional increase in muscular tone

Involves increased tone in “anti-gravity” muscles

In the upper extremities, resistance to stretching out biceps, but not triceps
In the lower extremities, resistance to stretching out quadriceps but not hamstrings

seen in upper motor neuron

Front 147

What is Rigidity? what is it seen in?

(o)

Back 147

Seen in Parkinson’s disease and other extrapyramidal disorders

A bi-directional increase in tone to passive range of motion

The resistance to passive range of motion is relatively independent of degree of force or rate of speed

Front 148

What is Paratonia? commonly seen in?

(o)

Back 148

feels like the pt is trying to stop you from moving the limb

Commonly seen in dementia

Also known as gegenhalten (to hold against)

A bidirectional resistance to passive range of motion that increases with force and rate of movement, as if voluntary

Front 149

Loss of power in greater proportion than clumsiness
Hypotonia
Muscle atrophy
Muscle fasciculations

what type of lesion?

(o)

Back 149

Lower Motoneuron

Front 150

Compare Duchenne, Facioscapulohumeral, and Limb girdle Muscular dystrophies for the following characteristics:
Age of onset
Sex
Pseudohypertorphy
Initial distribution
Involvement of the face
Rate of progression
Contractures and deformity
Inheritance

(o)

Back 150

Front 151

what is the genetic defect in duchenne muscular dystrophy?

Back 151

Dystrophin gene on short arm of X chromosome codes for dystrophin protein, which is a cytoskeletal structural protein.

this is damaged

Front 152

a boy presents to your office and on physical exam you note that their calves are pretty toned. Mom says that when the boy is on the ground he does this strange thing where he arches his back and climbs his way off the ground...what is this called? sign of?

Back 152

Gower's sign

in Duchenne

Front 153

you are in your neuro office and examining a young lady patient who has issues with smiling. You ask her to smile and she physically can't. Her forehead is unwrinkeld and the corners of her mouth do not curl. On physical exam, you note winging of the scapula. What does this pt have?

Back 153

Facioscapulohumeral Muscular Dystrophy

One key gene is on the long arm of chromosome 4. The function of the gene product is as yet unknown.

Front 154

a man presents to you with a seemingly triangular face. On a hunch, you hit their hypothenar eminence with your reflex hammer and it causes their thumb to move towards their pinky. To confirm what you think, you have the pt squeeze your hand and tell them to open it as soon as you tell them. When you say go, their hand stays in a grip...what do they have? What is the genetics going on?

Back 154

Myotonic Dystrophy
A gene near the centromere of chromosome 19 codes for myotonic dystrophy protein kinase. In M.D. dozens to hundreds of “CTG” repeats occur in the gene. The transcribed mRNA gets trapped within the cell’s nucleus.

Front 155

what happens in Myasthenia gravis physiologically?

(o)

Back 155

antibodies to the AChR

Front 156

pt presents to your office with muscle weakness. They say they are fine in the morning, but by the end of the day they have drooping eyelids, jaw drop, and drooling...what do they likely have?

Back 156

MG

Front 157

what are some of the associated dz with MG? what is the most important one?

Back 157

THYMOMA (malignant mediastinal tumor)

thyroid disease

widespread immune complex disease

Front 158

what is a polyneuropathy

(o)

Back 158

Bilaterally symmetric
Distinct from mononeuropathy and multiple mononeuropathies

so the key is that you have to have the deficit on the same spot on both sides

mulitple mononeuorpathies would be like radial on one side, ulnar on the other

poly is like whole left and right hand (stocking and glove is a common characteristic of polyneuopathy)

Front 159

Distal-greater-than-proximal weakness
Distal-greater-than-proximal numbness
A “stocking-glove” pattern of weakness, numbness or both
“Length-dependent” neuropathy
Disrupts DTRs more than other forms of lower-motoneuron weakness

this describes?

(o)

Back 159

Polyneuropathy

the longer the axon the worse it is affected

Front 160

Werdnig-Hoffman is a motoneuron disease affecting what population?

*

Back 160

NEONATES

you will see characteristic FROG LEG position and floppy baby
(other thing that causes floppy baby? Botulin toxin)

BABIES WILL NOT HAVE REFLEXES

Front 161

a 60 year old man presents to your office and says that he cannot do routine tasks such as going up steps, getting out of a chair, or swallowing. You note widespread atrophy. What do you suspect...

Back 161

Amyotrophic Lateral Sclerosis

ALS

Front 162

Back 162

note: here is the prime example for the following
myopaty=duchenne
motor neuron dz= ALS

Front 163

of the following, which will have a MARKEDLY increase CK level?

Myopathy
MG
Polyneuropathy
Motorneuron disease

Back 163

Myopathy

(think duchenne's muscular dystrophy)

Front 164

Back 164

Front 165

. The student will be able to measure and record visual acuity according to generally agreed upon conventions

Back 165

Eye chart for visual acuity testing. Standard distances are 20 feet for a wall chart and 14 inches for a hand-held card.

Read down to the smallest characters possible or until reaching the 20/20 line, whichever comes first. The acuity is the last line correctly read.

say they read like all of the letters but miss 1 or 2 you say 20/20 minus (assuming they read at the 20 20 line)

Front 166

a cut at the optic nerve would cause what visual problem?

Back 166

Front 167

a cut at the optic chiasm would cause what visual problem?

Back 167

Front 168

a cut at the right optic tract would cause what visual problem?

Back 168

left homonomous hemianopia

Front 169

right temporal damage could cause what visual damage?

Back 169

4

Front 170

post central gyrus=?

pre=?

Back 170

post central=somatosensory

pre= motor

Front 171

please diagram the light reflex pathway...is this PNS or SNS?

Back 171

CN II

pretectal nucleus

Edinger Westphal nucleus

ciliary ganglion

contract pupil

(This is PNS)

Front 172

please diagram out the sympathetic pathway for pupilary dilation

Back 172

ipsilateral hypothalamus

synapse at T1 (IML)

travel up the sympathetic chain and to the apex of the lung (look out for horners)

goes to carotid bifurcation but then sends to the pupil for dilation

Front 173

how can a tumor of the apex of the lung lead to pupil issues?

Back 173

this is horner's syndrome due to a pancoast tumor

you will see a constricted pupil because the sympathetics (which would normally dilate the pupil) stop at the apex of the lung and are disrupted by the tumor

Front 174

pt presents with a droopy eyelid and constricted pupil...

Back 174

ipsilateral sympathetic chain issue--HORNERS

miosis-small pupil

ptosis- droppy eyelid

Front 175

please list the primary and secondary action of the extraocular muscles. consider what would happen with a lesion

Back 175

Front 176

What do CN 6 and 4 do?

Back 176

LR6SO4

LR (lateral rectus) connected to CN 6
SO (superior oblique) connected to CN 4
Remaining EOMs and levator palpebrae connected to CN 3

Front 177

right lower face is weak, upper face is fine

is this an upper or lower motor neuron problem

(o)

Back 177

UPPER

Front 178

right lower face is weak, upper face is also weak

is this an upper or lower motor neuron problem

(o)

Back 178

LOWER

Front 179

The student will be able to grade muscular strength according to the MRC (Medical Research Council) scale.

(o)

Back 179

Front 180

functions of the insular lobe

Back 180

emotions, drives, drug addiction etc

Front 181

just list the cranial nerves and their functions

Back 181

* I-Olfactory nerve,
* II-Optic nerve,
* III-Oculomotor nerve,
* IV-Trochlear nerve/pathic nerve,
* V-Trigeminal nerve/dentist nerve
* VI-Abducens nerve,
* VII-Facial nerve,
* VIII-Vestibulocochlear nerve/Auditory nerve,
* IX-Glossopharyngeal nerve,
* X-Vagus nerve,
* XI-Accessory nerve/Spinal accessory nerve and
* XII-Hypoglossal nerve.

Front 182

Dorsal horn is associated with what?

Ventral?

Back 182

Dorsal: Sensory

Ventral Motor

Front 183

consider the locations of white and gray matter in the spinal cord and brain (which is deep and which is superficial in each)

Back 183

spinal cord: gray matter deep

brain: gray matter superficial

Front 184

what is the difference btw the gracile and cuneate fasiculate

Back 184

Gracile: carries axons from lower extremities

cuneate: upper (t6 and up)

REMEMBER: Feet in the grass

Part of the DCML pathway for sensory info (proprioception, vibration, fine touch)

Front 185

please diagram out the DCML pathway...what info does this carry?

Back 185

Front 186

please diagram out the Anterior Lateral System, and list what it carries

Back 186

Front 187

Please diagram out fine touch and vibration of the face

Back 187

Front 188

please diagram orofacial pain and temp

Back 188

Front 189

The left optic tract carries info from what visual field?

Back 189

right visual field

Front 190

where will superior visual field info end up?

Back 190

inferior calcarine fissure

(remember they also travel inferior in the meyers loop)

Front 191

a pituitary tumor causes pressure on the optic chiasm...what will this lead to?


****TEST

Back 191

Bitemporal hemianopia

Will only be able to see info from medial visual fields (peripheral vision lost-->tunnel vision)

Front 192

Back 192

Front 193

pt falls off their bike and was not wearing a helmet. They now say that they have lost vision just in the very center of each eye...what is going on?

Back 193

Central scotomas

Front 194

diagram out the corticospinal and corticobulbar tracts

Back 194

Front 195

pt has flaccid paralysis...what is the problem

Back 195

lower motor neuron

Front 196

pt has spastic paralysis...what is the problem?

Back 196

upper motor neuron

Front 197

middle cerebral artery damage will lead to issues in what structure

Back 197

face

comes out of sylvian fissure and branches like a tree

Front 198

anterior cerebral artery damage will lead to issues in what structure

Back 198

legs and feet

Front 199

describe the role of the Direct pathway and the indirect pathway in the basal ganglia

**TEST

Back 199

Direct pathway: starting movement

indirect pathway: stopping movement

Front 200

which pathway (direct or indirect) encourages GPm activity...what does this do?

Back 200

INDIRECT

GPm has tonic inhibition of the thalamus (which is always wanting to activate movement...it's like GO GO GO)

thus the indirect by activating GPm will stop movement (this is the key thing to remember)

note: in the direct pathway, you inhibit GPm so inhibiting the inhibition leads to activity

Front 201

FIRST AID REVIEW QUESTION

abdominal pain radiating to the back, weight loss, migratory thrombophlebitis and obstructive jaundice should make you think what?

Back 201

Pancreatic adenocarcinoma

more common in pancreatic head

aggressive (prognosis is 6 months or less)

CEA and CA19-9 tumor markers

assoc with Cigarettes and chronic pancreatitis but not EtOH

Front 202

FIRST AID REVIEW QUESTION

What are some of the causes of aplastic anemia?

Back 202

Radiatoin and drugs (Benzene, chloramphenicol, alkylating agents, antimetabolites)

Viral agents (B19 parvo, EBV, HIV, HCV)

Fanconi's anemia

Idiopathic